BY: DR. MARWA SHAALAN - PowerPoint PPT Presentation

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  1. Angina Pectoris Definition Types of Angina BY: DR. MARWA SHAALAN Management of Angina Antianginal drugs MAIN EXIT NEXT

  2. Myocardial Blood Flow Myocardial O2 Demands Definition : Transient Myocardial ischemia Angina Pectoris Severe Chest pain 2 BACK MAIN EXIT INDEX NEXT

  3. Definition : Chest pain caused bytransient myocardial ischemiadue to animbalance betweenmyocardial oxygen supply and demand. 3 BACK MAIN EXIT INDEX NEXT

  4. Types of Angina 1. Stable Angina. 2. Unstable Angina. 3. Variant Angina. 4 BACK MAIN EXIT INDEX NEXT

  5. 1.Stable Angina . The commonest cause isADVANCED ATHEROSCELEROSIS Retrosternal pain Radiating to left arm & shoulder Lasting less than 15 min. HOME 5 BACK MAIN EXIT INDEX NEXT

  6. Stable Angina Relieving factors Predisposing factors Exertion Rest Emotion sublingual nitroglycerin Exposure to cold weather Heavy meals 6 BACK MAIN EXIT INDEX NEXT

  7. Stable Angina Anginal pain is often associated with Depression of ST segment Exercise ECG showing typical severe down sloping ST segment : Standing 7 min. 9 min. 1 min. 3 min. In between attacks :ECG is entirelyNORMAL 7 BACK MAIN EXIT INDEX NEXT

  8. 2.Unstable Angina . Increased frequency, severity or duration of pain in a patient of Stable Angina N.B. Pain occurs with less exertion or at rest Myocardial infarction may occur in 10-20% of patients. 8 BACK MAIN EXIT INDEX NEXT

  9. The underlying cause is Fissuring of atheroscelerotic plaques Platelet aggregation Thrombosis Coronary artery spasm • Atheroscelerotic changes 9 BACK MAIN EXIT INDEX NEXT

  10. 3.Variant Angina . (Prinzmetal) Chest pain at rest due to coronary artery spasm ECG changes: Return of the ST segment to the baseline after nitroglycerin administration With chest pain , marked ST segment elevation The baseline ECG Acute elevation of ST segment 10 BACK MAIN EXIT INDEX NEXT

  11. Management of Angina Management of Stable Angina Management of Unstable Angina Management of Variant Angina 11 BACK MAIN EXIT INDEX NEXT

  12. A-Management of Stable Angina 1- General measures. 2- Drug Treatment. 3- Coronary artery revascularization. 12 BACK MAIN EXIT INDEX NEXT

  13. General measures Treat Hypertension , Hypercholestrolimia and Diabetes Stop smoking Reduce weight AVOID Severe exertion Heavy meal Emotions Cold Weather • Graduated exercise may open new collaterals 13 BACK MAIN EXIT INDEX NEXT

  14. Drug Treatment a.For an acute attack b.For immediate pre-exertional prophylaxis c.For long-term prophylaxis d.Antiplatelet therapy. 14 BACK MAIN EXIT INDEX NEXT

  15. Persistence of pain Relief within 1-3 min. Treatment of an acute attack of angina 1-Sublingual nitroglycerin (0.5 mg ) or isosorbidedinitrate (5 mg ) or Oral spraynitroglycerin (0.4 mg/metered dose), isosorbidedinitrate(1.25 mg/metered dose) Repeat nitroglycerin at 5 min. interval (3 tab. max.) Relief not relieved Infarction HOSPITALIZATION 15 BACK MAIN EXIT INDEX NEXT

  16. 2-Immediate pre-exertional prophylaxis of Angina Sublingual nitroglycerin (0.5 mg) or isorbide dinitrate (5 mg) should be taken 5 min.beforeeffort. 3-For Long term prophylaxis: Long acting nitrates, Ca++ channel blockers, b-blockers or combinations of these drugs. 4-Antiplatelet therapy: Aspirin in small dose (75-150 mg daily orally) or Dipyridamole (75 mg t.d.s orally) 16 BACK MAIN EXIT INDEX NEXT

  17. Coronary Artery Revascularization Coronary artery bypass grafting (CABG) Percutaneous Transluminal coronary Angioplasty (PTCA) For patients not responding to adequate medical therapy 17 BACK MAIN EXIT INDEX NEXT

  18. B-Management of Unstable Angina Nitrate + b-blocker + Aspirin (low dose) and/or Heparin or Thrombolytic (stryptokinase) to minimize risk of infarction 18 BACK MAIN EXIT INDEX NEXT

  19. C-Management of Variant Angina Nitrates and/or Ca++Channel blockers For the acute attack & prophylaxis 19 BACK MAIN EXIT INDEX NEXT

  20. What are the antianginal drugs? 1-Organic nitrates. 2-- adrenoceptor blockers. 3-Calcium channel blockers. 20 BACK MAIN EXIT INDEX NEXT

  21. Relaxation of smooth muscles Dilatation 1-Organic Nitrates NITRATES Veins Arteries 21 BACK MAIN EXIT INDEX NEXT

  22. Cellular Mechanism of Vasodilatation Formation of Nitric oxide (NO) Nitrates Activation of Guanylate cyclase Synthesis of cyclic GMP Relaxation of Vascular smooth muscles N.B. (-SH) groups are required for formation of NO. 22 BACK MAIN EXIT INDEX NEXT

  23. Effect of Nitrates : On Stable Angina : Arteriolar dilatation Venodilatation 1- Preload Afterload Myocardial Oxygen demand 2-Redistribution of coronary flow towards subendocardium 3- Dilatation of coronary collateral vessels.

  24. On Variant Angina : Relax smooth muscles of the epicardial coronaries  relieve coronary artery spasm On Unstable Angina : Dilatation of epicardial coronary arteries + reducing O2 demands 24 BACK MAIN EXIT INDEX NEXT

  25. Preparations : Short acting For acute attacks Long acting For antianginal prophylaxis Nitroglycerin oral SR (6.25-12mg) 2-4 times/day - 2% ointment (1-1.5 inch/4hrs) - patches (1 patch=25mg)/day Isosorbide dinitrate (oral) 10-40mg t.d.s. Isosorbide mononitrate (oral) 20mg/12 hrs. Nitroglycerin (sublingual, buccal spray) Isosorbide dinitrate(sublingual, buccal spray) 26 BACK MAIN EXIT INDEX NEXT

  26. Duration of Action of Various Preparations of Organic Nitrates

  27. 6- Prolonged high dose Methaemoglobinaemia Adverse Reactions : 1- Postural Hypotension & Syncope 2- Tachycardia 3- Drug Rash 4- Facial Flushing 5- Throbbing Headache 28 BACK MAIN EXIT INDEX NEXT

  28. The main limitation of chronic nitrate therapy is TOLERANCE Tolerance to the antianginal effect occurs as a result of chronic administration How does it occur? It develops as SH groups in vessel wall become oxidized by constant exposure to nitrates, this prevents the production of NO & hence stimulation of Guanylate cyclase which is believed to be fundamental to smooth muscle relaxation produced by the drugs. “NITRATE FREE INTERVAL” of 8-10 hrs reduces or prevents development of nitrate tolerance.e.g. isosorbide dinitrate is given at 7am, noon and 5pm; trnsdermal patches should be used for about 12 hrs daily 29 BACK MAIN EXIT INDEX NEXT

  29. What are nitrosamines & what is their medical importance ? These are small molecules formed from the combination of nitrates and nitrites with amines. They are also found in tobacco and cigarette smoke. Some of them may cause cancer in humans, but there is no evidence that the small doses of nitrates used in treatment of angina result in significant body levels of nitrosamines. What is the effect of nitroglycerin on platelet aggregation ? It decreases platelet aggregation. 30 BACK MAIN EXIT INDEX NEXT

  30. 2-Beta-Adrenoceptor Blocker b-blockers are effective in STABLE & UNSTABLE angina In contrast they are notuseful for vasospastic angina (Variant) {Prinzmetal}& may worsen the condition. This deleterious effect is likely due to an increase in coronary resistance caused by the unopposed effects of catecholamines acting at a-adrenoceptors.

  31. Mechanism of antianginal action: The effectiveness of b-adrenoceptor blockers in the treatment of exertional angina is attributable to a fall in myocardial O2 requirement at rest & during exertion due to : 1- A -vechronotropic effect (particularly during exercise). 2- A -veinotropic effect. 3- A reduction in arterial blood pressure (particularly systolic pressure) during exercise. 32 BACK MAIN EXIT INDEX NEXT

  32. Rate & contractility Systolic ejection period & left ventricular end diastolic vol. Myocardial O2 requirements Undesirable effects of b-blockers in treatment of angina: However the net effect of b-blockers is to  myocardial O2 requirementparticularly during exercise; their potentially deleterious effects can be balanced by concomitant use of nitrates 33 33 BACK MAIN EXIT INDEX NEXT

  33. Drug Route Dosage Propranolol Oral 30-360 mg/day in 2-4 divided doses Nadolol Oral 40-80 mg ONCE daily Atenolol Oral 50-100 mg ONCE daily Metoprolol Oral 50-100 mg TWICE daily Dosage and Route of Administration

  34. Adverse Reactions : Bronchospasm CHF A-V block Cold extremities Worsening symptoms of PVD Hypotension 35 BACK MAIN EXIT INDEX NEXT

  35. Plasma Triglycerides & HDL Cholesterol Adverse Reactions : Fatigue & weakness Mask signs of Hypoglycemia Nightmares , Hallucinations , Depression. Discontinuation after long ttt exacerbates Angina 36 BACK MAIN EXIT INDEX NEXT

  36. Contraindications : Bronchial asthma CHF A-V block Hypotension Peripheral Vascular disease 37 BACK MAIN EXIT INDEX NEXT

  37. 3-Calcium Channel-Blockers Used in treatment of all types of angina. Verapamil(80-160 mg) /8 hr Diltiazem(60-120 mg) /8 hr Dihydropyridine group Nifedipine (10-40mg) /8 hr Amlodipine 5mg/day 38 BACK MAIN EXIT INDEX NEXT

  38. Block Voltage -dependent calcium channels (L-type) in cardiac and smooth muscles. CALCIUM

  39. Mechanism of anti-anginal action : 1 - Coronary artery dilatation and relief of coronary spasm (variant angina) 2 -Decrease myocardial O2 demand due to: • Arteriolar dilatation Vascular resistance Afterload • (Verapamil & Diltiazem) • Decrease HR. • Decrease contractility • Decrease AV conductivity

  40. Dosage and Route of Administration

  41. Adverse reactions : Ankle edema Dizziness Headache Hypotension Constipation Reflex Tachycardia with Nifedipine Flushing A-V block & HF onlywith Verapamil & Diltiazem

  42. Contraindications of Verapamil & Diltiazem: 2 -Sinus or A-V node disease. 1 -HF 3 -Bradycardia.

  43. Combination Therapy in Angina Pectoris ? Verapamil or Diltiazem + Nitrate b-blocker + Long acting Nitrate ? ? b-blocker + Nitrate + Nifedipine b-blocker + Nifedipine ?

  44. b-blockers block reflex tachycardia produced by nitrates • Nitrates attenuate the increased left ventricular end-diastolic volume associated with b-blockers

  45. b-blockers decrease reflex tachycardia produced by nifedepine.

  46. Verapamil or Diltiazem decrease tachycardia produced by nitrates. • In patients with stable angina not controlled by two types of antianginal drugs the use of three agents may provide improvement.